论文部分内容阅读
目的 :探讨运动与心脏重塑的生物学机制中心肌细胞内游离钙的动态变化。方法 :采用激光扫描共聚焦显微技术 ,对不同运动负荷条件下小鼠心肌活细胞内游离钙浓度的变化进行观察、记录和分析 ,采用多道生理记录仪经颈动脉插管 ,对不同运动负荷条件下小鼠心肌收缩功能进行记录与分析。结果 :与对照组比较 ,有氧运动组心脏发生肥大 ,左室内压力二阶导数增加了 47 1 7%(P <0 0 0 1 ) ,表明心肌收缩功能增强 ,静息期心肌细胞内游离 [Ca2 + ]i 基值无显著性变化 ,峰值显著性增加了 1 5 7 2 % (P <0 0 0 1 ) ,达峰时间延长了 3 8 5 % (P <0 0 0 1 ) ;大强度疲劳组心肌肥大 ,但心肌收缩功能降低 (-3 5 2 4% ,P <0 0 0 1 ) ,静息期心肌细胞内游离 [Ca2 + ]i 基值和峰值分别显著增加了 41 9% (P <0 0 0 1 )和 2 0 6 3 % (P <0 0 0 1 ) ,达峰时间延长了 74 8% (P <0 0 0 1 )。有氧运动组与大强度疲劳组比较 ,心肌细胞内游离 [Ca2 + ]i 峰值和达峰时间均有显著性差异 (P <0 0 0 1 )。结论 :不同运动负荷影响心肌细胞内游离 [Ca2 + ]i 的变化 ,大强度疲劳训练可导致心肌细胞内游离[Ca2 + ]i 和静息态基值大幅度升高 ,峰值后移
Objective: To investigate the dynamic changes of intracellular free calcium in the biological mechanism of exercise and cardiac remodeling. Methods: Laser scanning confocal microscopy was used to observe, record and analyze the changes of intracellular free calcium concentration in living myocardium of mice under different exercise load. The carotid artery was cannulated with multi-channel physiology recorder to measure the changes of intracellular free calcium Myocardial contractile function was recorded and analyzed under the condition of loading. Results: Compared with the control group, cardiac hypertrophy was found in aerobic exercise group and the second derivative of left ventricular pressure was increased by 47 1 7% (P <0.01 01), indicating that myocardial contractile function was enhanced and intracellular free myocardial cells were released at rest Ca2 +] i had no significant change, the peak value increased by 1572% (P <0.01), the peak time prolonged by 385% (P <0.01) Myocardial hypertrophy in the fatigue group, however, decreased myocardial contractile function (-3 5 2 4%, P 0 01), basal cell free [Ca 2 +] i at rest and peak amplitude increased 41 9% P <0 0 0 1) and 2 0 6 3% (P <0 0 0 1), the peak time prolonged 74 8% (P 0 01). There were significant differences in peak and peak of free [Ca2 +] i in cardiomyocytes between aerobic exercise group and high intensity fatigue group (P <0.01). CONCLUSION: The changes of free [Ca2 +] i in cardiomyocytes were affected by different exercise loads. High-intensity fatigue training resulted in a significant increase in intracellular free [Ca2 +] i and resting cardiomyocytes,